A host of cellular processes enable plants to defend themselves from disease caused by pathogenic agents. These processes apparently form an integrated set of resistance mechanisms that is activated by initial infection and then limits further spread of the invading pathogenic microorganism.
Subsequent to recognition of a potentially pathogenic microbe, plants can activate an array of biochemical responses. Generally, the plant responds by inducing several local responses in the cells immediately surrounding the infection site. The most common resistance response observed in both nonhost and race-specific interactions is termed the "hypersensitive response" (HR). In the hypersensitive response, cells contacted by the pathogen, and often neighboring cells, rapidly collapse and dry in a necrotic fleck. Other responses include the deposition of callose, the physical thickening of cell walls by lignification, and the synthesis of various antibiotic small molecules and proteins. Genetic factors in both the host and the pathogen determine the specificity of these local responses which can be very effective in limiting the spread of infection.
Many environmental and genetic factors cause general leaf necrosis in maize and other plants. In addition, numerous recessive and dominant genes have been reported which cause discreet necrotic lesions to form. These lesion mutants mimic disease lesions caused by various pathogenic organisms of maize. For example, Les1, a temperature-sensitive conditional lethal mutant, mimics the appearance of Helminthosporium maydis on susceptible maize.
Many genes causing necrotic lesions have been reported. The pattern of lesion spread on leaves is a function of two factors: lesion initiation and individual lesion enlargement.
The lethal leaf spot-1 (lls1) mutation of maize is inherited in a recessive monogenic fashion and is characterized by the formation of scattered, necrotic leaf spots (lesions) that expand continuously to engulf the entire tissue. Since lls1 spots show striking resemblance to lesions incited by race 1 of Cochliobolus (Helminthosporium) carbonum on susceptible maize, this mutation has been grouped among the class of genetic defects in maize called "disease lesion mimics."Lesion mimic mutations of maize have been shown to be specified by more than forty independent loci. These lesion mimic plants produce discreet disease-like symptoms in the absence of any invading pathogens. It is intriguing that more than two thirds of these mutations display a partially dominant, gain-of-function inheritance, making it the largest class of dominant mutants in maize, and suggesting the involvement of a signalling pathway in the induction of lesions in these mutations. Similar mutations have also been discovered in other plants including arabidopsis and barley.
Despite the availability of the large number of lesion mimic mutations in plants, the mechanistic basis and significance of this phenomenon, and the wild-type function of the genes involved, has remained elusive. The understanding of the molecular and cellular events that are responsible for plant disease resistance remains rudimentary. This is especially true of the events controlling the earliest steps of active plant defense, recognition of a potential pathogen and transfer of the cognitive signal throughout the cell and surrounding tissue.
Diseases are particularly destructive processes resulting from specific causes and characterized by specific symptoms. Generally the symptoms can be related to a specific cause, usually a pathogenic organism. In plants, a variety of pathogenic organisms cause a wide variety of disease symptoms. Because of the lack of understanding of the plant defense system, methods are needed to protect plants against pathogen attack.